Comprehensive modeling of the Correa cascade in precancerous lesions of gastric cancer: Leveraging animal, cellular, and organoid systems for translational insights

Figure 2 Representative experimental models for each stage of the Correa cascade, from chronic and atrophic gastritis to intestinal metaplasia, dysplasia, and early gastric cancer. It includes: (1) Animal models: N-methyl-N’-nitro-N-nitrosoguanidine-induced lesions in rats, Helicobacter pylori-infected mice, and spasmolytic polypeptide-expressing metaplasia models induced by tamoxifen or genetic modification; (2) Cellular models: Human gastric epithelial cell lines (e.g., gastric epithelial cell-1) exposed to chemical, inflammatory, or infectious stimuli to simulate precancerous changes; and (3) Organoid models: Patient-derived organoids from intestinal metaplasia or dysplastic tissue, pluripotent stem cell-derived gastric organoids via directed differentiation, and organoids from genetically engineered mice. Together, these models offer complementary platforms for investigating the stage-specific pathogenesis, immune responses, and therapeutic targets of precancerous gastric lesions. H. pylori: Helicobacter pylori; S. anginosus: Streptococcus anginosus; MNNG: N-methyl-N’-nitro-N-nitrosoguanidine; MNU: N-Nitroso-N-methylurea; PSC: Pluripotent stem cell.